In this report, transfection of tau plasmids into human neuroblastoma SK-N-SH cells caused a significant reduction in the messenger RNA (mRNA) levels of several Kv channels, including Kv2.1, Kv3.1, Kv5.1, Kv9.2, and KCNH4.

RECENT ADVANCES: Oxidative regulation of the delayed rectifier Kv2.1 and the Ca(2+)- and voltage-sensitive BK channel are established, but recent studies contest how their redox sensitivity contributes to altered excitability, progression of neurodegenerative diseases, and healthy aging.

K(+) efflux mediated by KV2.1 delayed rectifier K(+) channels, a predominant form of β cell KV channels, brings about the downstroke or repolarization phase of the action potential, which acts as a brake for insulin secretion owing to shutting down the CaV channel-mediated Ca(2+) entry.

We have obtained evidence that syntaxin-1A physically interacts with Kv2.1 (the predominant Kv in beta-cells) and the sulfonylurea receptor subunit of beta-cell K(ATP) channel to modify their gating behaviors.